Evidence map›Paper›PMID 31594933›Full record

ArticleNature communications2019

Context-specific regulation of surface and soluble IL7R expression by an autoimmune risk allele.

Hussein Al-Mossawi, Nicole Yager, Chelsea A Taylor, Evelyn Lau, Sara Danielli, Jelle de Wit, James Gilchrist, Isar Nassiri, Elise A Mahe, Wanseon Lee and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 55 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 1 country.

Hussein Al-MossawiNuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0002-2312-3754
Nicole YagerNuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Chelsea A TaylorDepartment of Oncology, Weatherall Institute of Molecular Medicine, Oxford, UK.
Evelyn LauWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Sara DanielliDepartment of Oncology, Weatherall Institute of Molecular Medicine, Oxford, UK.
Jelle de WitNuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0003-2444-6050
James GilchristWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Isar NassiriDepartment of Oncology, Weatherall Institute of Molecular Medicine, Oxford, UK.
Elise A MaheDepartment of Oncology, Weatherall Institute of Molecular Medicine, Oxford, UK.
Wanseon LeeWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Laila RizviNuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Seiko MakinoWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Jane CheesemanOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK.
Matt NevilleOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0002-6004-5433
Julian C KnightWellcome Centre for Human Genetics, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0002-0377-5536
Paul BownessNuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Benjamin P FairfaxDepartment of Oncology, Weatherall Institute of Molecular Medicine, Oxford, UK. benjamin.fairfax@oncology.ox.ac.uk.ORCID http://orcid.org/0000-0001-7413-5002
Centre for Human Genetics · GBMRC Weatherall Institute of Molecular Medicine · GBNuffield Orthopaedic Centre · GBUniversity of Oxford · GB

Funding

Wellcome Trust 201488/Z/16/ZWellcome Trust 204969/Z/16/Z
6 · The paper itself

Abstract

IL-7 is a key factor in T cell immunity and common variants at IL7R, encoding its receptor, are associated with autoimmune disease susceptibility. IL7R mRNA is induced in stimulated monocytes, yet a function for IL7R in monocyte biology remains unexplored. Here we characterize genetic regulation of IL7R at the protein level in healthy individuals, and find that monocyte surface and soluble IL7R (sIL7R) are markedly induced by lipopolysaccharide. In monocytes, both surface IL7R and sIL7R expression strongly associate with allelic carriage of rs6897932, a disease-associated IL7R polymorphism. Monocytes produce more sIL7R than CD4 + T cells, and the amount is additionally correlated with the expression of DDX39A, encoding a splicing factor. Synovial fluid-derived monocytes from patients with spondyloarthritis are enriched for IL7R

Indexed as

AllelesAutoimmunityDEAD-box RNA HelicasesGene Expression ProfilingGenetic Predisposition to DiseaseHealthy VolunteersHumansInterleukin-7Interleukin-7 Receptor alpha SubunitLipopolysaccharidesMonocytesPolymorphism, Single NucleotideSequence Analysis, RNASingle-Cell AnalysisSpondylitis, AnkylosingSynovial FluidDDX39A protein, humanDEAD-box RNA HelicasesIL7 protein, humanIL7R protein, humanInterleukin-7Interleukin-7 Receptor alpha SubunitLipopolysaccharides

Identifiers

PMID31594933
PMCPMC6783569
OpenAlexW2980051151

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.